That's what a lot of people do (without the aspirin) and it works fine and is much more economical than blends. The aspirin is a mild uncoupler of mitochondrial respiration, like t3 or DNP, only MUCH weaker. The problem with aspirin is that according to a couple of recent studies, blocking PGF2 alpha production with aspirin or other NSAIDs impairs post exercise protein synthesis in muscle. I would skip the aspirin.

It's gotten harder to get the white cross ephedrines. The distributors want a copy of your driver license and SS card. That sounds like a prescription for identity theft to me.

That's what a lot of people do (without the aspirin) and it works fine and is much more economical than blends. The aspirin is a mild uncoupler of mitochondrial respiration, like T3 or DNP, only MUCH weaker. The problem with aspirin is that according to a couple of recent studies, blocking PGF2 alpha production with aspirin or other NSAIDs impairs post exercise protein synthesis in muscle. I would skip the aspirin.

It's gotten harder to get the white cross ephedrines. The distributors want a copy of your driver license and SS card. That sounds like a prescription for identity theft to me.

ALso, Aspirin is a prostaglandin inhibitor. It works by inhibiting cyclooxygenase activity. Because certain prostaglandins act to inhibit lipolysis and are produced in response to adrenergic stimulation, prostaglandin inhibitors have the potential to enhance ephedrine’s actions on fat loss. Nandi's theories are interesting,because the data does suggest that Aspirine enhances the thermogenic effects of ephedrine.Also, White crosses are hard to find because people use them to make Crystal Meth!

Aspirin as a promoter of ephedrine-induced thermogenesis: potential use in the treatment of obesity.

Dulloo AG, Miller DS.

Chronic administration of aspirin to obese mice had no effect on energy balance and body composition. In contrast, ephedrine increased energy expenditure by 9% and reduced body weight and body fat by 18% and 50%, respectively: obesity, however, was reduced but not reversed. In the presence of both ephedrine and aspirin, increase in energy expenditure found during treatment with ephedrine alone was doubled, and the obese group lost greater than 75% of body fat: obesity was reversed. These studies indicate that although aspirin administered alone has no influence on energy balance it can markedly potentiate thermogenic properties of ephedrine, effects which led to a normalization of body composition of the obese to that of the lean. Such ephedrine-aspirin mixtures, often found in over-the-counter preparations for asthma and bronchial disorders, could be put to new use as aids for treatment of human obesity.

Ephedrine, caffeine and aspirin: safety and efficacy for treatment of human obesity.

Daly PA, Krieger DR, Dulloo AG, Young JB, Landsberg L.

Dept of Medicine, Harvard Medical School, Boston.

The safety and efficacy of a mixture of ephedrine (75-150mg), caffeine (150mg) and aspirin (330mg), in divided premeal doses, were investigated in 24 obese humans (mean BMI 37.0) in a randomized double blind placebo-controlled trial. Energy intake was not restricted. Overall weight loss over 8 weeks was 2.2kg for ECA vs. 0.7 kg for placebo (p < 0.05). 8 of 13 placebo subjects returned 5 months later and received ECA in an unblinded crossover. After 8 weeks, mean weight loss with ECA was 3.2 kg vs 1.3 kg for placebo (p = 0.036). 6 subjects continued on ECA for 7 to 26 months. After 5 months on ECA, average weight loss in 5 of these was 5.2 kg compared to 0.03 kg gained during 5 months between studies with no intervention (p = 0.03). The sixth subject lost 66 kg over 13 months by self-imposed caloric restriction. In all studies, no significant changes in heart rate, blood pressure, blood glucose, insulin, and cholesterol levels, and no differences in the frequency of side effects were found. ECA in these doses is thus well tolerated in otherwise healthy obese subjects, and supports modest, sustained weight loss even without prescribed caloric restriction, and may be more effective in conjunction with restriction of energy intake.

It would be interesting to see the results in the research that nandi posted using half of the amount of the maximum otc doses. That is the problem with some of these studies,, as we know some things are very dose dependant.

Good references guns! , sounds like the jury s still out. lipolysis vs protein systhesis, wonder what the effect of a gram of test would have these studies.......

Department of Nutrition and Dietetics, King's College, University of London, Kensington, UK.

OBJECTIVE: To determine whether or not aspirin further potentiates the greater post-prandial thermogenesis induced by ephedrine with caffeine. DESIGN: Determination of the acute metabolic rate response to the following treatments: 1050 kJ liquid meal (M); meal plus ephedrine (30 mg) and caffeine (100 mg) (MEC) or meal plus ephedrine, caffeine and aspirin (300 mg) (MECA). SUBJECTS: Lean, pre-disposed obese and obese women (n = 10 each group). MEASUREMENTS: Pre- and post-treatment metabolic rate determinations via indirect calorimetry. Post-treatment measurements made at 20 min intervals for a total of 160 min. RESULTS: In all groups, metabolic rate increased significantly more following the MEC or MECA, compared to the meal only (p < 0.05). The obese group had a significantly greater absolute increase in metabolic rate following the MECA and MEC compared to both the lean and pre-disposed obese groups (p < 0.05). Metabolic rate remained elevated at the end of the 160 min following all treatments. CONCLUSION: Aspirin does not further potentiate the acute thermic effect of ephedrine and caffeine with a meal. However, the full thermogenic response was not measured and longer duration studies are necessary to confirm these results.

Yeah, see again with that study the sample group was very small and the study was based on rate of thermogenesis following a meal. I would like to see a bigger study as well as a longer time line, not to mention without having just ingested a meal (although that isn't as big of a deal). Most other studies has a MUCH longer time line than 160 minutes.The study does conflict with the vast majority of research on aspirin, ephedrine and caffeine, which raises some question marks.

Considering that the doses of aspirin people take as part of the ECA stack are so small compared to the NSAID doses they used in those muscle studies, the aspirin in ECA is probably pretty harmless. And you are right, the bulk of the data show aspirin does enhance thermogenesis.

It has always been my understanding that the reason for aspirin was to extend the duration of the stimulant effects produced by the other two drugs. This has been my experience upon removal of the aspirin from the stack,which I did several months ago after reading one of those studies Nandi cited earlier in this thread.

Salicylate, the main metabolite of acetylsalicylic acid, is a classical uncoupler of oxidative phosphorylation. This is responsible for some aspects of aspirin's toxicity as well as the mild thermogenic effect it is supposed to exert as part of the ECA stack.

I took it out of my ECA combo after reading the muscle and PGF studies, but who knows if the low doses are detrimental to gains.

The picture is even more complicated by a couple of studies that I came across this afternoon (1) (2).

Tumor Necrosis Factor alpha is a proinflammatory cytokine released by certain white blood cells that has been implicated in AIDS wasting and cancer cachexia. Before now its mechanism of action has been unknown. The first paper shows that TNF inhibits the local production of IGF-1 in skeletal muscle.

The second paper showed that low dose aspirin inhibits the release of TNF-alpha into the circulation from leukocytes.

Moreover, although there are conflicting studies, a number have shown that strenuous exercise elevates levels of TNF:

dan duchaine wrote that taking aspirin before w/o could reduce cortisol reducing inflamations.but is it true?is cortisol released in response to muscle-damege or is it released in response to pro-inflammatory PG production?